Molecular aspects of inflammatory and immune responses in Alzheimer's disease.
Neurobiol Aging
; 17(5): 687-93, 1996.
Article
en En
| MEDLINE
| ID: mdl-8892341
ABSTRACT
Recent advances indicate numerous molecular and cellular elements of the immune system are involved in the pathogenesis of Alzheimer's disease. Amyloid beta protein deposition induces many molecules associated with a predominantly local inflammatory response within the brain parenchyma. These responses also provoke the release of immune system mediators including cytokines, which all seem largely to be produced by reactive cells such as astrocytes and microglia. Classical acute phase proteins of the pentraxin and serine protease inhibitor (serpin) families as well as a host of complement proteins and some coagulation factor seem the most intrinsically involved. These secreted molecules display variable binding with the amyloidotic lesions. Although our understanding of the molecular specificity and significance of the interaction of these proteins within the lesions is not replete, the development of unique inhibitors of the inflammatory reactions could provide therapeutic strategies to impede the pathogenetic process. Currently, this appears a more viable option than to inhibit amyloid beta production or modify amyloid beta precursor protein processing, an approach which seems more complex.
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Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Mediadores de Inflamación
/
Enfermedad de Alzheimer
/
Inflamación
Límite:
Humans
Idioma:
En
Revista:
Neurobiol Aging
Año:
1996
Tipo del documento:
Article
País de afiliación:
Estados Unidos